In-Depth Reports - Atherosclerosis causes

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Atherosclerosis causes

Atherosclerosis is a condition in which deposits of fatty material, called plaques, develop in the walls of arteries, leading to a reduction or blockage of blood flow. It can affect almost any artery in the body. Atherosclerosis is the most important and most common type of arteriosclerosis, a group of diseases in which the wall of an artery becomes thicker and less elastic.

The development of atherosclerosis is complex, but the primary event appears to be injury to the arterial wall. Many different factors can injure the artery's wall, triggering the formation of plaque, for example, turbulent blood flow due to high blood pressure (BP), inflammatory immune responses, certain infections, and chemical abnormalities of the blood, such as diabetes and high cholesterol.

Chemical signals that are generated as a result of injury cause white blood cells to attach to the arterial wall, where they collect cholesterol and other fatty material, eventually forming plaque. Over time, the build-up of plaque narrows the space within an artery.

Certain risk factors, such as being a male, advanced age, and a family history of early atherosclerosis, cannot be changed. However, to help prevent atherosclerosis, individuals can refrain from tobacco use, decrease low density lipoprotein (LDL) cholesterol levels, lower blood pressure, lose weight, consume fresh fruits and vegetables daily, eat a diet that is low in saturated fats, and exercise regularly.

Diabetic individuals need to maintain strict control of their blood sugar. People at high risk for developing atherosclerosis may also benefit from taking certain drugs, such as statins, aspirin, or other antiplatelet drugs.

Review Date: 5/27/2024
Reviewed By: Michael A. Chen, MD, PhD, Associate Professor of Medicine, Division of Cardiology, Harborview Medical Center, University of Washington Medical School, Seattle, WA. Also reviewed by David C. Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.

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